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Autosis: a new form of cell death in myocardial ischemia-reperfusion injury.
Yang, Xiaoting; Wu, Hui; Zhou, Gang; Zhang, Dong; Yang, Qingzhuo; Liu, Yanfang; Li, Yi.
Afiliação
  • Yang X; Institute of Cardiovascular Diseases, China Three Gorges University, Yichang, 443003, HuBei Province, China.
  • Wu H; Department of Cardiology, Yichang Central People's Hospital, Yiling Road 183, Yichang, 443000, HuBei Province, China.
  • Zhou G; HuBei Clinical Research Center for Ischemic Cardiovascular Disease, Yichang, HuBei Province, China.
  • Zhang D; Central Laboratory, The First College of Clinical Medical Science, China Three Gorges University & Yichang Central People's Hospital, Yichang, HuBei Province, China.
  • Yang Q; Hubei Key Laboratory of Ischemic Cardiovascular Disease, Yichang, HuBei Province, China.
  • Liu Y; Institute of Cardiovascular Diseases, China Three Gorges University, Yichang, 443003, HuBei Province, China. wuhui@ctgu.edu.cn.
  • Li Y; Department of Cardiology, Yichang Central People's Hospital, Yiling Road 183, Yichang, 443000, HuBei Province, China. wuhui@ctgu.edu.cn.
Mol Cell Biochem ; 2024 Apr 09.
Article em En | MEDLINE | ID: mdl-38594455
ABSTRACT
Cardiomyocytes undergo a variety of cell death events during myocardial ischemia‒reperfusion injury (MIRI). Understanding the causes of cardiomyocyte mortality is critical for the prevention and treatment of MIRI. Among the various types of cell death, autosis is a recently identified type of autophagic cell death with distinct morphological and chemical characteristics. Autosis can be attenuated by autophagy inhibitors but not reversed by apoptosis or necrosis inhibitors. In recent years, it has been shown that during the late phase of reperfusion, autosis is activated, which exacerbates myocardial injury. This article describes the characteristics of autosis, autophagic cell death, and the relationship between autophagic cell death and autosis; reviews the mechanism of autosis in MIRI; and discusses its clinical significance.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Base de dados: MEDLINE Idioma: En Revista: Mol Cell Biochem Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China